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Biomedical subjects

M Buti

Publications and source records attributed to M Buti.

At least 109 records · Page 6Linked to original sources
PubMed1987

Anti-HD IgM as a marker of chronic delta infection.

The value of anti-HD IgM as a marker of chronic delta infection was evaluated by correlating its presence in serum with that of HD-Ag in liver cells and with the degree of inflammatory activity. Thirty-six patients with HBsAg-positive chronic hepatitis and anti-HD at high titers were studied. Overall, the liver cells of 26 patients contained HD-Ag and 27 were positive for IgM anti-HD. The correlation between both markers was excellent: 25 cases were positive for both serum anti-HD IgM and intrahepatic HD-Ag and 8 were negative for both markers. There was only 1 HD-Ag-positive patient, who was anti-HD IgM-negative. Two patients were anti-HD IgM-positive and HD-Ag-negative. Histological damage was more severe in anti-HD IgM-positive cases than in those negative for this marker (Knodell's index 13.5 vs 11.9, P less than 0.01). We conclude that anti-HD IgM is a good marker of chronic active delta infection.

Adolescent↗
PubMed1987

Clinical and serological outcome of acute delta infection.

To assess the clinical and serological outcome of hepatitis delta virus (HDV) infection, 59 patients with acute delta hepatitis were followed for 6-28 months. Forty-two patients had simultaneous HDV and HBV coinfection (anti-HBc IgM-positive, group I) and 17 were HBsAg carriers with HDV superinfection (anti-HBc IgM-negative, group II). Overall, serum HD-Ag and anti-HD IgM were the most sensitive markers for diagnosis of delta infection during the first 2 weeks after onset of symptoms. The clinical presentation was similar in both groups; 4 patients (1 in group I and 3 in group II) (7%) developed fulminant hepatitis, but none of them died. The majority of patients with HBV-HDV coinfection (group I) eventually recovered, whereas all HBsAg carriers with HDV superinfection (group II) developed chronic liver disease. Liver histology in these patients showed chronic active hepatitis and/or cirrhosis in 90%. The hepatic lesion was probably due to persistent HDV infection, as indicated by the presence of intrahepatic HD-Ag and/or persistence of serum anti-HD IgM in 90% of the patients.

Antibodies, Viral↗
PubMed1986

Serological diagnosis of acute delta hepatitis.

Sixty-three intravenous drug addicts with HBsAg positive hepatitis were studied to evaluate the diagnostic usefulness of hepatitis delta virus (HDV) markers for diagnosis of acute HDV infection. Patients were tested for HBsAg, anti-HBc-IgM, and anti-HD-IgM by radioimmunoassay (RIA), and for hepatitis delta antigen (HD-Ag) by a commercial enzyme-linked immunoassay (ELISA). At least two serum samples at a mean interval of 4 wk were examined from each patient. HDV markers were found in 41 cases. In the first serum sample (obtained within 1-5 wk after onset of illness) HD-Ag was found in 32 cases and was the only HDV marker in 22; in the remaining 10 cases, HD-Ag was found along with total anti-HD, and in 6 of them anti-HD-IgM was also detected. Five additional patients were only positive for total anti-HD, and anti-HD of the IgM class was the only marker in one patient. HD-Ag was found more often in the patients studied during the first 2 wk of illness. In the second serum sample, HD-Ag was never the only marker detected, seven patients were still positive, and in all of them anti-HD was also present. Thirty patients were only positive for anti-HD. Seroconversion from HD-Ag to anti-HD occurred in 20 of 22 (91%) patients. The results suggest that HD-Ag determination by ELISA in the initial serum sample, during the first 2 wk of illness, may be the most sensitive test for the diagnosis of acute delta infection, and that seroconversion to anti-HD usually occurs after the sixth week of illness.

Acute Disease↗
PubMed1986

Immunoprophylaxis of perinatal transmission of the hepatitis B virus: efficacy of hepatitis B immune globulin and hepatitis B vaccine in a low-prevalence area.

One hundred eleven newborn infants born of Spanish hepatitis B surface antigen (HBsAg) carrier mothers were consecutively assigned to one of three treatment groups. Group A was treated with three or four doses of hepatitis B immune globulin (HBIG) in one of three different schedules. Group B received one dose of hepatitis B vaccine (Hevac-B, Pasteur) at birth and at 1, 2 and 12 months. Group C was treated with the same vaccination schedule as group B and in addition received a single dose of HBIG at birth. Comparisons were made in the 85 babies who had strictly completed the immunization schedule and had been followed for at least 12 months. The three immunization protocols were equally effective, since none of the children became a chronic HBsAg carrier or developed acute symptomatic infection. There were five transient and subclinical infections among children who received only HBIG (group A), one transient infection in group B, and one in group C. There seems to be some correlation between anti-HBs levels and degree of protection, since all transient infections in group A occurred in the subgroups who did not maintain protective antibodies during the first 6 months. Although the percentage of responders in the two vaccinated groups did not differ significantly, children who received only vaccine reached higher antibody levels than those who also received HBIG. Our results suggest that any immunization schedule able to maintain anti-HBs levels during the first 6 months of life would be useful to prevent mother-to-infant transmission of the hepatitis B virus in areas where most of the carrier women are expected to be anti-HBe positive and hence relatively less infectious.

Carrier State↗
PubMed1986

Prolonged inhibition of hepatitis B virus replication with vidarabine monophosphate in chronic active type B hepatitis.

Eight patients with chronic (mean 52 months) type B hepatitis (chronic active hepatitis and active cirrhosis) and markers of active viral replication (presence of HBeAg and HBV-DNA in serum) were treated with Ara-AMP for 7-12 weeks. The mean follow-up time was 18.3 months. All but one patient responded to treatment. In seven patients, HBeAg and HBV-DNA became negative and developed anti-HBe. One patient lost HBsAg as well as HBeAg and HBV-DNA. HBcAg in liver tissue became undetectable or greatly reduced in the seven patients in whom it was strongly positive. Aminotransferase and immunoglobulin levels reverted to normal in the seven responders and remained normal through the entire follow-up period. A second liver biopsy, performed after completion of therapy, showed improvement in six of eight cases, with disappearance of lobular activity. Two patients treated for 12 weeks developed a severe polyneuropathy lasting for 6 months. A 7-week course of Ara-AMP seems to induce long-lasting inhibition of viral replication, along with an improvement in liver function tests and liver histology, without significant side effects. On the other hand, a 12-week course was associated with the development of a severe and prolonged polyneuropathy.

Adult↗
PubMed1986

Diagnostic usefulness of anti-HBc-IgM and anti-HD antibodies in acute viral hepatitis.

To evaluate diagnostic improvement achieved with the determination of antibody to hepatitis core antigen of IgM type (anti-HBc-IgM) and antibody to delta antigen (anti-HD) in acute type B hepatitis, 155 patients (of whom 100 were drug addicts) were studied, using these markers in association with the classical markers of viral hepatitis (anti-HBc, anti-HBs, anti-HAV-IgM and anti-cytomegalovirus antibodies). With classical diagnostic criteria, 121 patients would have been diagnosed as having B hepatitis (HBs Ag and/or anti-HBc antibody positive without anti-HBs antibody), 33 non A non-B hepatitis (all markers negative or anti-HBc and anti-HBs positive) and 3 A hepatitis (anti-HAV-IgM antibody positive). With the current markers, 89 were B hepatitis (anti-HBc-IgM antibody positive), 18 were simultaneous B and D infections (anti-HBc-IgM and anti-HD antibodies positive), 6 were D hepatitis (anti-HBc-IgM antibody negative and anti-HD antibody positive), 39 non-A non-B hepatitis (anti-HBc-IgM, anti-HD, HAV-IgM and anti-cytomegalovirus antibodies negative) and 3 hepatitis A. Of the 121 cases initially diagnosed as B hepatitis, only 79 were actually B hepatitis, 16 were simultaneous B and D infections, 6 D hepatitis, 18 non-A non-B hepatitis and 2 A hepatitis. Of the 33 cases considered to be non A non-B hepatitis, only 21 were really non-A non-B hepatitis; 10 were B hepatitis and 2 B and D hepatitis. When anti-HBc-IgM and anti-HD antibodies were determined, the initial diagnosis was modified in 54 of 155 cases (35 p. 100).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗